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CRH promotes S. pneumoniae growth in vitro and increases lung carriage in mice.

Ndjom CG, Jones HP - Front Microbiol (2015)

Bottom Line: The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae.We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth.Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Medical Genetics, University of North Texas Health Science Center, Fort Worth, TX USA ; Center for Biotechnology Education, Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD USA.

ABSTRACT
Streptococcus pneumoniae (S. pneumoniae), a commensal across the nasal passages, is responsible for the majority of infectious pneumonia cases worldwide. Previous studies have shown that hormonal factors may be influential in regulating S. pneumoniae's transition from a non-pathogen to a pathogenic state. The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae. Mice were infected with CRH-treated S. pneumoniae via intranasal route, showing an increase in pulmonary bacterial burden. We also quantified S. pneumoniae's response to CRH through limited serial dilutions and growth curve analysis. We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth. Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH. These results demonstrate a role for CRH in S. pneumoniae pathogenicity, thus implicating CRH in mediating the transition of S. pneumoniae into a pathogenic state.

No MeSH data available.


Related in: MedlinePlus

Titer-dependent effects of CRH on S. pneumoniae colony formation. Ten-fold serial dilutions of S. pneumoniae were incubated in the absence (A) or presence of two concentrations of CRH, 2.1 × 10-4 μM (B) and 4.0 × 10-4 μM, (C) and plated on blood agar plates. Data shown is representative of two independent experiments (A). (B) Represents quantitation of the aforementioned results in (A). Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups. White bars denote unexposed S. pneumoniae, gray and black bars denote S. pneumoniae exposed to two different CRH concentrations, 4.0 × 10-4 μM and 2.0 × 10-4 μM, respectively (B). (C) Highlights the specificity of CRH compared to its homolog UCN. Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.
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Figure 2: Titer-dependent effects of CRH on S. pneumoniae colony formation. Ten-fold serial dilutions of S. pneumoniae were incubated in the absence (A) or presence of two concentrations of CRH, 2.1 × 10-4 μM (B) and 4.0 × 10-4 μM, (C) and plated on blood agar plates. Data shown is representative of two independent experiments (A). (B) Represents quantitation of the aforementioned results in (A). Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups. White bars denote unexposed S. pneumoniae, gray and black bars denote S. pneumoniae exposed to two different CRH concentrations, 4.0 × 10-4 μM and 2.0 × 10-4 μM, respectively (B). (C) Highlights the specificity of CRH compared to its homolog UCN. Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.

Mentions: The above results suggested that CRH directly promotes the pathogenicity of S. pneumoniae by increased colonization in the lung. We assessed the effect of CRH on S. pneumoniae proliferation controlling for bacterial titer and variation in CRH concentration. S. pneumoniae colony forming units (CFUs) were significantly higher (P ≤ 0.05) given exposure to both concentrations of CRH at each titer of S. pneumoniae. In contrast to un-treated cultures of S. pneumoniae, CRH significantly sustained detection of CFUs at the lowest titer (8th-fold dilution; Figures 2A,B). To confirm specificity of CRH’s effect, additional experiments were performed whereby S. pneumoniae was exposed to the CRH homolog UCN. Lower concentrations of UCN (2.1 × 10-4mM/μl) were also used in testing. No differences in CFUs were observed in the presence of UCN at different concentrations compare to untreated S. pneumoniae (Figure 2C).


CRH promotes S. pneumoniae growth in vitro and increases lung carriage in mice.

Ndjom CG, Jones HP - Front Microbiol (2015)

Titer-dependent effects of CRH on S. pneumoniae colony formation. Ten-fold serial dilutions of S. pneumoniae were incubated in the absence (A) or presence of two concentrations of CRH, 2.1 × 10-4 μM (B) and 4.0 × 10-4 μM, (C) and plated on blood agar plates. Data shown is representative of two independent experiments (A). (B) Represents quantitation of the aforementioned results in (A). Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups. White bars denote unexposed S. pneumoniae, gray and black bars denote S. pneumoniae exposed to two different CRH concentrations, 4.0 × 10-4 μM and 2.0 × 10-4 μM, respectively (B). (C) Highlights the specificity of CRH compared to its homolog UCN. Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 2: Titer-dependent effects of CRH on S. pneumoniae colony formation. Ten-fold serial dilutions of S. pneumoniae were incubated in the absence (A) or presence of two concentrations of CRH, 2.1 × 10-4 μM (B) and 4.0 × 10-4 μM, (C) and plated on blood agar plates. Data shown is representative of two independent experiments (A). (B) Represents quantitation of the aforementioned results in (A). Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups. White bars denote unexposed S. pneumoniae, gray and black bars denote S. pneumoniae exposed to two different CRH concentrations, 4.0 × 10-4 μM and 2.0 × 10-4 μM, respectively (B). (C) Highlights the specificity of CRH compared to its homolog UCN. Bars represent mean (N = 3) ± SE. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.
Mentions: The above results suggested that CRH directly promotes the pathogenicity of S. pneumoniae by increased colonization in the lung. We assessed the effect of CRH on S. pneumoniae proliferation controlling for bacterial titer and variation in CRH concentration. S. pneumoniae colony forming units (CFUs) were significantly higher (P ≤ 0.05) given exposure to both concentrations of CRH at each titer of S. pneumoniae. In contrast to un-treated cultures of S. pneumoniae, CRH significantly sustained detection of CFUs at the lowest titer (8th-fold dilution; Figures 2A,B). To confirm specificity of CRH’s effect, additional experiments were performed whereby S. pneumoniae was exposed to the CRH homolog UCN. Lower concentrations of UCN (2.1 × 10-4mM/μl) were also used in testing. No differences in CFUs were observed in the presence of UCN at different concentrations compare to untreated S. pneumoniae (Figure 2C).

Bottom Line: The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae.We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth.Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Medical Genetics, University of North Texas Health Science Center, Fort Worth, TX USA ; Center for Biotechnology Education, Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD USA.

ABSTRACT
Streptococcus pneumoniae (S. pneumoniae), a commensal across the nasal passages, is responsible for the majority of infectious pneumonia cases worldwide. Previous studies have shown that hormonal factors may be influential in regulating S. pneumoniae's transition from a non-pathogen to a pathogenic state. The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae. Mice were infected with CRH-treated S. pneumoniae via intranasal route, showing an increase in pulmonary bacterial burden. We also quantified S. pneumoniae's response to CRH through limited serial dilutions and growth curve analysis. We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth. Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH. These results demonstrate a role for CRH in S. pneumoniae pathogenicity, thus implicating CRH in mediating the transition of S. pneumoniae into a pathogenic state.

No MeSH data available.


Related in: MedlinePlus